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Gynaecology STG > Gynacological Tumours and Cancers > Flashcards

Gynacological Tumours and Cancers Flashcards

1
Q

Cervical Intraepithelial Neoplasia

A

precursor lesion for Cervical Ca; Requires persistent HPV infection to develop; High risk HPV strains include 16, 18, 31 and 33

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2
Q

Transformation Zone

A

Endocervix comprises thin Secretory Glandular Epithelium which meets the Ectocervix Stratified Squamous Epithelium at the Squamocolumnar Junction
o Under influence of Oestrogen, Glandular Epithelium pushed out into Ectocervix, where due to the lower Ph, undergoes Metaplasia =Transformation Zone
▪ TZ typically Ectocervical in women of reproductive age, while it is Endocervical in Post-menopausal women
o High Mitotic Activity of TZ is vulnerable to HPV-driven change

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3
Q

Dyskaryosis

A

Cytological Dx – Primary screening tool; Markers include NCR, Shape and Density of Nucleus, Inflammation, Infection or Mitoses

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4
Q

Colposcopy

A

Magnified Visualisation of TZ after applying 5% Acetic Acid or Lugol’s Iodine
o Abnormalities are Punched Biopsied or definitively treated
If Cancer suspected, do not treat with LLETZ as can cause bleeding, and compromise further treatment
o CIN appears as ‘Acetowhite Epithelium’, with Vascular abnormalities, especially Mosaic and Punctuating; Grossly abnormal vessels suggestive of Microinvasive

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5
Q

CIN

A

Histological Dx – Characterised by loss of Differentiation and Maturation of Basal Layer; CIN I – III Based on Thickness of abnormality

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6
Q

Management of CIN 1

A

Spontaneously regresses in 50-60% within 2yrs; Low malignant potential, but 10-fold higher than normal cytology
o Conservative monitoring with Colposcopy/Cytology 6/12ly, or LLETZ if persistent

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7
Q

Management of high grade CIN

A

High Grade CIN (>I) – Progresses to cancer in 3-5% of CIN II and 20-30% of CIN III within 10yrs;
LLETZ is recommended

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8
Q

Complications of LLETZ

A

Haemorrhage, Infection, Vaso-vagal Reaction, Anxiety; In longer term, Cervical Stenosis, Incompetence and Risk of Premature Delivery can occur (rarely)

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9
Q

Follow up after LLETZ

A

If Low grade, Cytology and HPV testing at 6/12; If normal, return to 3yrly; If High grade, Cytology and High-risk HPV Test of Cure at 6/12; if normal, return to 3yrly

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10
Q

NHS Cervical Screening Programme

A

• Smear Test Screening to pick up CIN, which progresses to Cancer
o 3yrly for women 25 – 50yrs; If normal, then 5yrly between 51 – 64
• If Borderline or Mild Dyskaryosis – Testing for High-risk HPV subtypes
o If High risk subtypes present, or if Abnormal Cytology – For Colposcopy
• If normal Smear – Follow up in 3yrs

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11
Q

Cervical Cancer Stats

A

Second most common cancer in women worldwide; Mortality decreasing due to Screening
o Dual peaks of incidence 30-39yrs, and >70yrs
o Screening changes disease trend towards Microscopic disease and Adenocarcinoma

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12
Q

Risk Factors for Cervical Cancer

A

Overwhelming majority associated with Persistent, high risk HPV infection; Other RF include Smoking (reduces viral clearance) and Immunosuppression

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13
Q

Cervical Ca Presentation

A

Presents at Screening and Treatment of CIN, Post-coital Bleeding, Post-Menopausal Bleeding (Although more likely to be Endometrial Ca); Rarely presents as Vaginal Bleeding, Ureteric Obstruction, Weight loss, Bowel Disturbance and Fistulas (Vesicovaginal most commonly)

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14
Q

Assessment of Cervical Cancer

A

U/Es, LFTs, FBCs; CT AP for staging; MRI Pelvis; Examination Under Anaesthesia
• FIGO Staging system – Based on Diameter/Size, Involvement of Pelvic Sidewall, Extent of
Vagina, Extension between True Pelvis, Bladder/Bowel Involvement or Distant mets

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15
Q

Treatment of Cervical Cancer: Stage 1a1

A

Local excision or TAH

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16
Q

Treatment of Cervical Cancer: Stage 1a2 and 1b2

A

Check for LN involvement with pelvic lymphadenectomy

FZ or Paraffin in two-stage; If LN negative, Wertheim’s Hysterectomy

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17
Q

Treatment of Cervical Cancer: Fertility Sparing Surgery

A

E.g. Radical Trachelectomy for early stage disease if LN negative
o Increased risk of Late miscarriage, PPROM,
Preterm delivery

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18
Q

Treatment of Cervical Cancer: Stage 1b2 +

A

Stage Ib2 (>4cm) and IIa (Beyond Uterus) – CRT, Lymphadenectomy and Wertheim’s
• >Ib2 – Combination Chemoradiotherapy
• Stage IVb – Chemotherapy, Radiotherapy, Best Supportive Care, Palliative RT

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19
Q

Ovarian Cancer

A

Leading cause of death from gynaecological malignancy; 90% Epithelial Ovarian Cancer
o Peak incidence 75 – 84yrs
• Believed to be due to irritation of Surface Epithelium by damage during ovulation;

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20
Q

Risk Factors for Ovarian Cancer

A

COCP halves risk, Nulliparity, Early Menarche/Late Menopause increases risk
• Genetic Risk – BRCA1, BRCA2, HNPCC (Lynch Syndrome)
o Surveillance with CA125/TVS (Efficacy not proven); Prophylactic surgery (BSO ± TAH)

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21
Q

Mature Cystic Teratoma

A

Mature Cystic Teratoma (=Dermoid Cyst) – Common benign tumours typically occurring in premenopausal age group; Asymptomatic but rupture is painful
o Teratomas are Germ Cell Tumours which form normal tissue structures
o Most Teratomas contain elements derived from all three Embryonic layers
o Typically, Cystic tumours lined with Skin with Underlying Sebaceous Glands and Hair Follicles; Cyst becomes filled with thick greasy Sebaceous Material and Hair

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22
Q

High Grade Serous Carcinoma

A

Most common Malignant Ovarian Tumour accounting for 70% of Ovarian Cancers; More commonly Solid and Cystic Components
o Composed of Pleomorphic cells with Hyperchromatic Nuclei with high NCR arranged in a Papillary architecture

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23
Q

High Grade Serous Carcinoma: Risk Factors

A

Number of Ovulations, Family History (5% Inherited Cancer Syndromes e.g. BRCA1/2 and Lynch Syndrome
o BRCA1/2 have 30-60% Lifetime Risk of developing Ovarian Ca

24
Q

High Grade Serous Carcinoma: Presentation

A

Might present with diverse, non-specific signs that only manifest if tumour is large; Pain, Abdominal Swelling, Anorexia, N+V, Weight Loss; Ascites, Pleural Effusion
o Patients usually present at high stage; Poor prognosis

25
Q

Presentation of Ovarian Cancer

A

Vague common symptoms which may be mistaken as IBS or Diverticular disease; Common symptoms include Bloating/Distention, Urinary Symptoms, Change in Bowel Habit, Abnormal Vaginal Bleeding or Pelvic Mass
• Ascites, Palpable Mass (Especially Omentum, common site of mets), Pleural Effusion, Supraclavicular LN (Virchow’s Nodes)

26
Q

Investigation of Ovarian Cancer

A

• FBC, U/Es, LFT, Albumin
• CA125 – Raised in 80% of Epithelial Cancers; Part of RMI (Factor of Ultrasound findings as 0, 1 or 3; and Menopausal Status as 1 or 3)
• CA19.9 raised in Mucinous tumours, which more likely have normal CA125
• Rarer tumour type markers – AFP, hCG, LDH, Inhibin and Oestradiol
• Imaging – Abdominal/Pelvic Ultrasound, CXR for Staging and Pre-op, CT AP for staging
o FIGO staging – Based on Local invasion, Pelvic Invasion, and Distant mets

27
Q

Management of Ovarian Cancer: Ascites

A

Management of Ascites – Sample should be sent for Cytology, Microbiology and Biochem; Drain with pig-tail drain under aseptic technique, with LA instillation

28
Q

Management of Ovarian Cancer: Staging

A

Staging Laparotomy through Midline Incision if high RMI; Should aim to remove as much tumour as possible (Optimal Debulking)
o TAH+BSO, Omentectomy, LN Sampling (Pelvic and Para-Aortic), Peritoneal Biopsies, Washing and Ascitic Sampling
o Full Staging important as it affects whether Adjuvant Chemo required

29
Q

Management of Ovarian Cancer: Chemo and Surgery

A

• Neoadjuvant and Adjuvant Chemo plus Interval Debulking Surgery for advanced disease
• Chemotherapy comprises 6 cycles Carboplatin ± Paclitaxel every 3wks
o Baseline CT, Creatinine Clearance (or EDTA Clearance), and Histological Diagnosis should be done prior to Chemotherapy
• Novel Agents being investigated include Anti-VEFG, Anti-EGFR, and TK Inhibitors

30
Q

Endometrial Hyperplasia

A

Premalignant condition; Predisposes/Associated with Endometrial Ca; Caused by Excessive Unopposed Oestrogen (Exogenous or Endogenous)

31
Q

Endometrial Hyperplasia: Presentation

A

Presents as Irregular menstruation, Post-menopausal Bleed or Investigations for Infertility

32
Q

Endometrial Hyperplasia: Classification

A

Degree of Hyperplasia depends on Glandular-Stroma ratio; Atypical Hyperplasia describes appearance of individual Glandular cells
o Atypical Hyperplasia – 46% of AH have concurrent Ca Endometrial; Recommend TAH (+BSO if >45yrs); Alternatively, if unfit for surgery or fertility desired, High-dose Progestagens plus 3 – 6 monthly re-biopsies
o Full Thickness Atypical Glandular Cells (without Stroma) =Endometrial Cancer

33
Q

Management of Endometrial Hyperplasia without Atypia

A
  • Exclude treatable causes of Unopposed Oestrogens – Oestrogen-only HRT, Oestrogen-secreting Tumour (E.g. Granulosa cell Ovarian tumours)
  • Progestagens – Continuous oral daily for 3 – 6/12, or IUS if post-menopausal
  • Simple Hyperplasia has 1% risk of progression; Complex (Adenomatous) 3.5%
  • Rebiopsy only if abnormal bleeding continues
34
Q

Endometrial Cancer

A

Predominantly affects Post-Menopausal Women (91% >50yrs); Caused by Excessive Unopposed Oestrogen (Similar Aetiology to Hyperplasia)

35
Q

Endogenous Sources of Oestrogen

A

Peripheral Conversion in Adipose tissue, Oestrogen-producing tumour, PCOS, Anovulatory cycles

36
Q

Exogenous Sources of Oestrogen

A

Oestrogen-only HRT, Tamoxifen (Oestrogen Agonism in Endometrium)

37
Q

Endometrial Cancer Risk Factors

A

Obesity and related (e.g.
T2DM, Hypothyroid, HTN), Nulliparity, PCOS, Early Menarche/Late Menopause, Genetic Predisposition (Lynch) and Breast Cancer (Shared lifestyle factors and Tamoxifen usage)
o Protective Factors – Parity, COCP (50% - 72% lower risk)

38
Q

Endometrial Cancer: Prognostic Factors

A

Major Prognostic factors are Grade (Differentiation) and FIGO staging

39
Q

Endometrial Cancer: Presentation

A

o Most present as Post-Menopausal Bleeding (1 in 10 of PMB); In Pre-menopausal, presents as Menstrual disturbance; 1% on routine Cervical Smear tests
o PV discharge and Pyometra instead of bleeding; 50% of Pyometra have Ca

40
Q

Endometrial Cancer: Investigations

A

TV USS (<4mm very low risk, sampling only if persistent bleeding; >4mm require sampling); Sampling either Blind or Hysteroscopy under LA or GA

41
Q

Endometrial Cancer: Treatment

A

TAH BSO and Pelvic Washing either Transverse or Midline Incision; Also, Laparoscopic
• Pelvic Lymphadenectomy – Role in low-grade, early disease is controversial
• Adjuvant RT – Brachytherapy for Intermediate risk; + EBRT in High risk or Locally advanced
• Hormone Therapy – High dose Progesterone for Advanced and Recurrent; Reduces bleeding and used for Palliation; No demonstrated survival advantage
• Palliative RT – Lower-dose, Fewer fractions of EBRT for Local Symptom control

42
Q

Pelvic Masses

A

Benign Adnexal Cysts in 34%; Leiomyoma (Fibroids) in 14%; 14% Malignancies, Dermoid Cyst in 13%, Endometriosis in 10%; Pelvic Inflammatory Disease and Pregnancy

43
Q

Uterine Fibroids

A

Most common benign tumours arising from Myometrium; =Leiomyomata, primarily composed of Smooth Muscle and may contain Fibrous tissue
o Unknown Aetiology but believed to be related to Oestrogen exposure
o 20 – 40% of women of Reproductive Age; Higher incidence in Afro-Caribbean and FH

o Described as Submucous, Intramural, Subserous, Cervical, Pedunculated

44
Q

Uterine Fibroids: Symptoms

A

o Many Asymptomatic; Can present with Dysmenorrhoea, Menorrhagia, Pressure Symptoms (especially Urinary Frequency) and Pelvic Pain; Infertility in <10%

45
Q

Uterine Fibroids: Treatment

A

No treatment if minimal symptoms; GnRH analogues may shrink Fibroids but typically neoadjuvant to surgery (Myomectomy) – Open, Laparoscopic or Hysteroscopic; Or Hysterectomy; Also, Uterine Artery Embo0lisation – Minimally invasive, avoids GA

46
Q

Benign Ovarian Tumours

A 
Follicular Cysts (<3cm), Corpus Luteal Cysts (<5cm)
o Use RMI to guide whether or not should be referred for cancer investigations
47
Q

Non-Gynaecological Causes of Masses

A

Bladder tumours, Intestinal Tumours, Diverticular Disease, IBD, Abscesses (Appendicitis), Lymphadenopathy

48
Q

Vulval Intraepithelial Neoplasia

A

More common in Post-Menopausal; Increasing incidence related to sexual practices
o Dysplastic Lesion of Squamous Epithelium; Associated with HPV infection, especially HPV16 (High risk); Associated with Smoking; CIN might also be present
o Up to 9% of VIN progresses to Vulval cancer

49
Q

Vulval Intraepithelial Neoplasia: Presentation

A

May present as Itch, Pain and Ulceration, but over 20% Asymptomatic; Lesions might be raised, Warty, Flat and Erythematous; Frequently Multifocal

50
Q

Vulval Intraepithelial Neoplasia: Diagnosis

A

Diagnosis by Punch Biopsy; Requires screening for Ca Cervix

51
Q

Vulval Intraepithelial Neoplasia: Management

A

VIN typically occurs as part of a field change, making removal complicated; High recurrence, even after radical vulvectomy
o Careful follow-up and biopsies of suspicious lesions
o Imiquimod stimulates immune system to clear genital warts; 5-FU no longer recommended due to ineffectiveness and poor tolerance
• Similar appearance to Adenocarcinoma-in-situ (Paget’s Disease of the Vulva); ~20% have invasive component, or underlying Adenocarcinoma (e.g. Colorectal)
o Excision and Rule out underlying malignancy

52
Q

Vulval Cancer

A

• Uncommon; 90% Squamous cell, 5% Melanoma; Most in Older women (Median 74yrs); Although younger women, especially if VIN, at risk
o Commonly arises on background of Lichen Sclerosus or VIN; FIGO Staging
o Presents as Tender Lump, Irritation or Bleeding; Might be obvious Ulcer
• Surgery is mainstay for Curative intent or Palliation; Wide Local Excision plus Groin LN dissection; Plastic reconstruction might be required
o Radiotherapy, Chemotherapy can be used Neoadjuvant or Adjuvant

53
Q

Vaginal Cancer

A

Rare; 1% of Gynaecological Malignancies; Most are mets from Cervical/Uterine or Vulval; True Vaginal Ca is mostly Squamous; Many previous Hx VAIN or other gynae cancers

54
Q

Vaginal Cancer: Predisposing Factors

A

Predisposing factors include Pelvic RT, Long term inflammation; Also, HPV related

55
Q

Vaginal Clear Cell Adenocarcinoma

A

Related to DES exposure In-Utero; Was previously given to pregnant women at risk of Miscarriage or Prem between 1940 – 1971; Critical time exposure in first half of pregnancy
o Wide Local Excision of early disease to preserve fertility; RT for advanced disease

Gynaecology STG (12 decks)

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